Toxoplasmosis is a ubiquitous infection in nature. It is characterized as a severe generalized or CNS granulomatous disease caused by Toxoplasma gondii. Asymptomatic infections are common; serologic surveys show that worldwide 25-50% of adult populations are infected and have detectable antibodies to the etiologic agent.
When the disease is acquired after birth, it may be associated with mild, nonspecific signs and symptoms, or it may be completely asymptomatic, with antibodies in patient's sera as the only indication of exposure. A more acute and sometimes fatal infection occurs in immunologically compromised patients.
Congenital infection, on the other hand, can be devastating. In animals, primary infection during pregnancy results in abortion or low fertility. In humans the clinical manifestations of congenital toxoplasmosis appear to be related to the trimester of pregnancy during which the mother acquired the infection. Infection during the first trimester is commonly associated with stillbirth, perinatal death, or the more severe forms of congenital toxoplasmosis. Infection during the third trimester usually results in mild or subclinical infection.
This clinical picture, together with the observation that Toxoplasma gondii trophozoites are rarely isolated from aborted fetuses, suggests that congenital toxoplasmosis syndromes may occur when the fetus is exposed either to the trophozoites and/or to a toxic substance produced by the infection.
The description of a toxic substance formed in vivo in mice infected with Toxoplasma gondii was first reported by Weinman and Klatchko, "Description of toxin in toxoplasmosis", Yale J. Biol. Med. 22: 323 (1950). This toxin, termed toxotoxin, was found in the peritoneal exudate and was demonstrated by intravenous inoculation into normal mice. When sufficient centrifuged supernatant of the exudate was injected, usually 0.1 to 0.5 ml, convulsions and immediate death resulted. These authors reported that toxotoxin was destroyed by trypsin and was nondialyzable. It was found to be stable at room and refrigerator temperatures and was not altered by lyophilization procedures. Activity was not reduced by heating to 56.degree. C. for 30 minutes, or to 100.degree. C., although autoclaving temperatures diminished potency.
Lunde and Jacobs in The Journal of Parasitology, Vol. 50, No. 1, February 1964, p.49-51 describe the preparation of a crude toxoplasma lysate obtained by lysing washed, filtered parasites in sterile distilled water. The toxic activity is destroyed by trypsin. The toxic material can be salted out with 30% saturated (NH.sub.4).sub.2 SO.sub.4 in the cold and has a high absorption peak at 260 M.mu.. Heating the lysate at 56.degree. C. for 15 minutes completely destroys its lethal effect. The lethal effect is noted only when the lysate is administered intraveneously to rabbits. Intraperitoneal inoculation in mice produced no effect.